2274 Splenic Infarction in Alcoholic Hepatitis

Abstract

INTRODUCTION: Case reports can be found in the literature describing elderly cirrhotic patients developing splenic infarctions (1,2). Herein, we describe a relatively young female who developed splenic infarction likely secondary to alcoholic hepatitis (AH). CASE DESCRIPTION/METHODS: A 40-year-old Caucasian female with past medical history of alcohol abuse and irritable bowel syndrome presented with jaundice, nausea, and vomiting. Laboratory showed ALT 54, AST 246, alkaline phosphatase 589, total bilirubin 14.0, INR 1.9, and ethanol level 240. WBC count was elevated to 20,900 with a 92% neutrophilic predominance. Leukocytosis was initially thought to be secondary to UTI as she also presented with urinary symptoms and urinalysis concerning for UTI. After a 5 day course of IV ceftriaxone, her WBC count decreased only to 18,400. Her abdominal exam began to worsen. RUQ ultrasound showed hepatic steatosis. CT scan with contrast showed moderate hepatomegaly and borderline splenomegaly with mild ascites. Abdominal pain, leukocytosis, and total bilirubin continued to worsen. Because of her severe abdominal pain and WBC count >50,000 despite a 7-day course of meropenem, contrast CT scan was repeated. At this time, lesions in the spleen concerning for infarction were seen. From here on, she was managed conservatively and her condition improved until discharge. DISCUSSION: Splenic function has been shown to decrease in patients with AH, but the exact pathophysiology is unclear (3). Splenic infarctions have been described in the literature in cirrhotic patients with co-morbidities (e.g. primary biliary cirrhosis), but to the authors’ knowledge there is not much mention in the literature of spontaneous splenic infarction in AH. In the right clinical context, physicians should consider splenic infarction in AH patients, especially in those with persistent leukocytosis which could be classified as a leukemoid reaction. Our report shows splenic vasculature infarction may be worth investigating in the future as an explanation for hyposplenia in AH.